Term
| Excitation of Striated Muscle |
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Definition
o Motor neuron fires, AP spreads to nerve terminals at Neuromuscular Junction
o Presynaptic release of ACh
o Activation of nicotinic receptors
o Increased Na+ and K+ conductance generates AP
o Action potentials in the muscle cell membrane are propagated to the T tubules by the spread of local currents. Thus, the T tubules are continuous with the sarcolemmal membrane and carry the depolarization from the surface to the interior of the muscle fiber.
o Depolarization of the T tubules causes a critical conformational change in its voltage-sensitive dihydropyridine receptor. This conformational change opens the Ca2+-release channels (ryanodine receptors) on the nearby sarcoplasmic reticulum. (As an aside, although the T tubules' dihydropyridine receptors are L-type voltage-gated Ca2+ channels, Ca2+ influx into the cell through these channels is not required for excitation-contraction coupling in skeletal muscle.)
o When these Ca2+-release channels open, Ca2+ is released from its storage site in the sarcoplasmic reticulum into the ICF of the muscle fiber, resulting in an increase in intracellular Ca2+ concentration. At rest, the intracellular free Ca2+ concentration is less than 10-7 M. After its release from the sarcoplasmic reticulum, intracellular free Ca2+ concentration increases to levels between 10-7 M and 10-6 M.
o Ca2+ binds to troponin C on the thin filaments, causing a conformational change in the troponin complex. Troponin C can bind as many as four Ca2+ ions per molecule of protein. Because this binding is cooperative, each molecule of bound Ca2+ increases the affinity of troponin C for the next Ca2+. Thus, even a small increase in Ca2+ concentration increases the likelihood that all of the binding sites will be occupied to produce the necessary conformational change in the troponin complex.
o The conformational change in troponin causes tropomyosin (which was previously blocking the interaction of actin and myosin) to be moved out of the way so that cross-bridge cycling can begin. When tropomyosin is moved away, the myosin-binding sites on actin, previously covered, are exposed.
o Cross-bridge cycling. With Ca2+ bound to troponin C and tropomyosin moved out of the way, myosin heads can now bind to actin and form so-called cross-bridges. Formation of cross-bridges is associated with hydrolysis of ATP
o Relaxation occurs when Ca2+ is reaccumulated in the sarcoplasmic reticulum by the Ca2+ ATPase of the sarcoplasmic reticulum membrane (SERCA). When the intracellular Ca2+ concentration decreases to less than 10-7 M, there is insufficient Ca2+ for binding to troponin C. When Ca2+ is released from troponin C, tropomyosin returns to its resting position, where it blocks the myosin-binding site on actin. As long as the intracellular Ca2+ is low, cross-bridge cycling cannot occur, and the muscle will be relaxed |
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Term
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Definition
| the muscle is allowed to develop tension at a preset length (called preload) but is not allowed to shorten (length is fixed). (Imagine trying to lift a 500-pound barbell. The tension developed would be great, but no shortening or movement of muscle would occur!) |
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Definition
| the forced is fixed but the length is allowed to shorten |
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Definition
| single contraction caused by a single action potential |
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Definition
| tension generated can be increased by increasing frequency of action potentials (twitch summation) |
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Definition
| the level of intracellular Ca2+ concentration remains high, resulting in continued binding of Ca2+ to troponin C and continued cross-bridge cycling. In this state, there is a sustained contraction called tetanus, rather than just a single twitch |
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Term
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Definition
= total tension – passive tension
• ~total tension is as measured during a maximal isometric contraction
• ~passive tension is tension produced by unstimulated muscle
*active tension at maximal length where there is maximal overlap between thick and thin filaments (most cross-bridges formed at rest)
• -preload is defined as the muscle length prior to contraction
*active tension increases with increasing preload, but then declines if muscle is stretched too much before contraction |
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Definition
| maximal at normal resting length |
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Definition
| slow twitch = slower contraction, but able to maintain tension during prolonged and repeated contractions e.g., posturemaintaining. Example: soleus muscle in leg requires 90 msec to develop peak tension |
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Definition
| = fast twitch = faster contraction, but also fatigue more rapidly due to dependence on glycolytic metabolism. Example: lateral rectus muscle of the eye reaches peak tension within 7.5 msec |
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Term
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Definition
(or unitary or visceral) muscle fibers are electrically connected to each other by gap junctions, so this type of smooth muscle is a functional syncytium
Form large muscle sheets in walls of gastrointestinal tract, bladder and uterus (blood vessels contain both types of smooth muscle)
Single-unit smooth muscle contracts in response to stretch
Single-unit smooth muscle can be active in the absence of nerve activity, through spontaneous pacemaker cells that can produce phasic contractions throughout the muscle, such as in the GI tract. This is referred to as myogenic activity. |
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Term
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Definition
do not have gap junctions with other smooth muscle fibers, so this type of smooth muscle is not syncytial
Contractions are initiated by released neurotransmitters (neurogenic)
Contractions are more discrete and localized. Can have twitches similar to those in skeletal muscle, but the duration of these is generally at least 10-fold longer than in skeletal muscle
Examples: iris, ciliary muscle, vas deferens
Anatomy: each multi-unit fiber is innervated by an en passant bouton, whereas in single-unit smooth muscle many fibers are not directly innervated but instead are activated by other fibers through gap junction |
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Term
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Definition
• Ca2+ for contraction comes mainly from ECF (or increased IP3)
• Troponin is not present
• Ca2+ binds to calmodulin to phosphorylate myosin
• Unlike in skeletal muscle, myosin must be phosphorylated for activation of myosin ATPase and cross bridging to actin for contraction.
• A latch bridge mechanism keeps cross-bridges between actin and myosin-II intact for sustained periods of time with a low energy requirement as long as Ca2+ remains somewhat elevated (e.g. by angiotensin II). The latch bridge allows for a persistent partial contraction (tonus) of smooth muscle. |
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Term
| Muscarinic receptor activation by ACh |
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Definition
1. In GI smooth muscle, decreases cAMP levels (M2 subtype) and activates phospholipase C increasing Ca2+ (M3 subtype) to cause contraction
2. In blood vessel epithelium, M3 increases nitric oxide (NO) which then relaxes vascular smooth muscle to decrease blood pressure. |
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Term
| Alpha-1 adrenergic receptor activation by NE |
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Definition
| smooth muscle of blood vessels increases IP3 and Ca2+ to increase contraction and increase blood pressure. |
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Term
| Beta-2 adrenergic receptor activation by Epinephrine |
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Definition
| smooth muscle of intestine or blood vessels increases cAMP to relax muscle and decrease peristalsis and blood pressure. |
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